Did you know? Aging does not compromise the inhibitory influence of the cardiopulmonary baroreceptors on blood pressure during exercise

Older people develop an exaggerated blood pressure (BP) during whole body exercise, which is associated with a higher risk of sudden cardiac death, myocardial infarction, future hypertension, cardiovascular disease, and left ventricular hypertrophy.¹ Since regular exercise is a common mitigating strategy for many health pathologies associated with aging, identification of the underlying mechanisms responsible for the exaggerated BP response is warranted in order to establish effective exercise prescription.

Blood pressure, both at rest and exercise, is regulated within a narrow range around a set value (operating point, OP) by the arterial baroreflex (ABR) via modulation of autonomic neural activity to the heart and vasculature.² As BP increases during exercise, the ABR is reset in direct relation to the exercise intensity, and regulates the elevated BP around the new OP.² The resetting of the ABR during exercise is mediated by activation and interaction of central and peripheral signals arising from higher brain centers (central command), exercising skeletal muscles (exercise pressor reflex) and the cardiopulmonary baroreceptors.^{3, 4}

In young healthy adults, loading of the cardiopulmonary baroreceptors during dynamic exercise inhibits the ABR resetting and lowers the prevailing BP during exercise,^{3, 4} presumably by providing a strong inhibitory influence on the muscle sympathetic nerve activity (MSNA). Considering that the interaction between cardiopulmonary baroreceptors and ABR is attenuated with aging,⁵ it is plausible that the exaggerated BP response to exercise in the elderly is due to an impaired cardiopulmonary baroreflex, such that attenuated inhibition of MSNA fails to adequately reset the ABR to a lower BP.

The effect of aging on the attenuating influence of the cardiopulmonary baroreceptors on the ABR resetting during exercise was evaluated by comparing the carotid-vasomotor baroreflex function curve in young (24 ± 1 years; n = 12) and older (71 ± 2 years; n = 12) healthy normotensive adults during upright and supine sub-maximal cycling that aimed to increase central blood volume, and thus load the cardiopulmonary baroreceptors. Both age groups, who were recreationally physically active 2–3 times per week but not systematically training, non-smokers and free from current medical symptoms, medication and history of major disease, signed informed consent to participate in accordance with the Declaration of Helsinki and was approved by the Copenhagen ethics committee (KF 01-186/02).

All subjects were familiarized with the experimental procedures, and abstained from eating for 2 h, caffeinated beverages for 12 h, and strenuous physical activity and alcohol for at least 24 h prior to the experimental session. Heart rate, BP and oxygen uptake (V̇O₂) were measured, as previously detailed.³ Carotid baroreflex (CBR) function was evaluated at rest and during cycling with application of variable carotid transmural pressures using the neck chamber method and derivation of carotid-vasomotor stimulus–response curves.³ Appropriate neck chamber placement was ensured by locating the carotid sinus bifurcation with ultrasound imaging, while older subjects were also screened for significant carotid artery plaques. Upright cycling began at low workload (~25 W) that increased within 3–5 min to an intensity corresponding to 50% HR reserve, while CBR function was assessed after 5–6 additional min to allow for steady-state to be established. Following sufficient recovery (at least 30 min), subjects repeated the exercise protocol in the supine position at a workload that elicited the same V̇O₂ as upright cycling. Oxygen consumption was kept constant during exercise in the two postures, in an attempt to maintain similar central command and activation of the exercise pressor reflex, and thus exclusively manipulate the load of the cardiopulmonary baroreceptors. Upright exercise was performed first in order to determine the V̇O₂ eliciting HR equivalent to 50% HR reserve, which was then used to determine the workload performed during supine cycling. The magnitude of exercise-induced baroreflex resetting was the sum of the changes in baroreflex curve parameters,⁶ and expressed as percent change to allow comparison between groups and conditions. One-way ANOVA with repeated measures was performed on the parameters of the curve fit to statistically compare the carotid-vasomotor stimulus–response curves across exercise conditions and Student–Newman–Keul's post hoc pair wise comparisons were used to locate group mean differences.

The magnitude of the upward and leftward resetting of the CBR-vasomotor stimulus response curve during upright exercise was ~50% larger in the older compared with the younger subjects (50 ± 9 vs. 75 ± 10 mmHg, young vs. older; p < 0.05). In contrast, the downward and leftward resetting of the CBR-vasomotor stimulus response curve during supine exercise was similar (~7%) in both groups (27 ± 3 vs. 36 ± 4 mmHg, young vs. older; p < 0.05). There was no difference in maximal gain of the stimulus–response curve during upright vs. supine cycling in either group, (0.50 ± 0.04 vs. 0.54 ± 0.03 mmHg⁻¹ young vs. older, respectively, Figure 1 and Table 1).

The present study provides novel insight regarding the effect of aging on the inhibitory influence of cardiopulmonary baroreceptors on carotid baroreflex resetting during dynamic exercise. In both young and older subjects, cycling in the supine position increased the load on the cardiopulmonary baroreceptors, and provoked a similar downward and leftward resetting of the CBR-vasomotor function curve as during upright cycling. Moreover, supine cycling significantly reduced the exercising blood pressure in both groups despite similar increases in oxygen uptake and relative heart rate, while the maximal gain of the CBR was maintained, thus presenting a mitigating alternative for the exaggerated BP during exercise in the elderly.

In conclusion, aging does not compromise the inhibitory influence of the cardiopulmonary baroreceptors on the arterial baroreflex function during exercise. The exaggerated BP response to exercise in the elderly cannot therefore be attributed to impaired cardiopulmonary baroreflex.

All authors were involved in the study conception, performed the experiments, analyzed the data, discussed the results and writing the paper. All authors contributed to the article and approved the submitted version.

This study was supported by The DanishHeart Foundation (03-1-3-69A-22074).